Fig. 6: HI-TOPK-032 inhibits cell proliferation by YB1/eEF1A1 signal pathways in EC.

a, b HI-TOPK-032 suppressed KYSE150 (a) and KYSE30 (b) cell viability. KYSE150 and KYSE30 cells were treated with various concentration of HI-TOPK-032 (0, 0.25, 0.5, 1, 2.5, 5 μM) and measured at 24, 48, 72 and 96 h. c, d HI-TOPK-032 suppressed anchorage-independent growth of KYSE150 (c) and KYSE30 (d) cells. KYSE150 and KYSE30 cells were treated with various concentration of HI-TOPK-032 (0, 0.25, 0.5, 1, 2.5, 5 μM) and measured after 7 days. e, f HI-TOPK-032 suppressed anchorage-dependent growth of KYSE150 (e) and KYSE30 (f) cells. KYSE150 and KYSE30 cells were treated with various concentration of HI-TOPK-032 (0, 0.25, 0.5, 1, 2.5, 5 μM) and measured after 10 days. g, h. HI-TOPK-032 decreased the mRNA level of eEF1A1 of KYSE150 (g) and KYSE30 (h) cells. KYSE150 and KYSE30 cells were treated with various concentration of HI-TOPK-032 (0, 0.25, 0.5, 1, 2.5, 5 μM). i, j The protein level of eEF1A1 and the phosphorylation levels of YB1, mTOR, AKT, and p70S6K were identified in KYSE150 (i) and KYSE30 (j) cells by Western blot. KYSE150 and KYSE30 cells were treated with various concentration of HI-TOPK-032 (0, 0.25, 0.5, 1, 2.5, 5 μM). All experiments were biological replicates and were repeated at least three times. Error bars showed standard error of the mean. *p ˂ 0.05, **p ˂ 0.01, ***p ˂ 0.001.